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RNA-seq experiment to investigate the effect of inactivating the Apoptosis Antagonizing Transcription Factor (Aatf)

ABSTRACT: RNA-seq experiment to investigate the effect of inactivating the Apoptosis Antagonizing Transcription Factor (Aatf)

PROVIDER: PRJEB27927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2713050_1.fastq.gz	Fastqsanger.gz
	ERR2713050_2.fastq.gz	Fastqsanger.gz
	ERR2713051_1.fastq.gz	Fastqsanger.gz
	ERR2713051_2.fastq.gz	Fastqsanger.gz
	ERR2713052_1.fastq.gz	Fastqsanger.gz

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RNA-seq experiment to investigate the effect of inactivating the Apoptosis Antagonizing Transcription Factor (Aatf)

Project description:Human nephronophthisis and related ciliopathies suggest a link between ciliary signaling defects and altered DNA damage responses. The goal of our study is to elucidate the molecular link of both signaling systems as well as the role of altered DNA damage responses in kidney degeneration and fibrosis. The kinase-regulated DNA damage response target Apoptosis Antagonizing Transcription Factor (Aatf) is a master regulator of the p53 response. Upon genetic deletion of Aatf in renal tubular cells we induce progressive renal failure and a phenotype closely resembling human nephronophthisis in mice and are able to show Aatf as a regulator of primary cilia and modulator of the DNA damage response connecting two pathogenetic concepts of nephronophthisis and nephronophthisis-related ciliopathies. The analysis of the RNA-sequencing of four Aatf-knockout mice and four wildtype mice supports the experimental findings.

2019-03-31 | E-MTAB-7077 | biostudies-arrayexpress

ChIP-seq following AATF in BIU-87 cells

Project description:With the increasing acknowledgment of the multifaceted roles of Anti-apoptotic Transcription Factor (AATF) in various cancers, our study directed its focus towards unraveling its implications in bladder cancer, particularly concerning the tumor microenvironment and immune landscape. We performed ChIP-seq to investigate the effect of AATF on chromatin status in BIU-87 cells.

2023-11-25 | GSE248243 | GEO

E-MTAB-7077

Project description:RNA-seq experiment to investigate the effect of inactivating the Apoptosis Antagonizing Transcription Factor (Aatf)

2019-01-22 | E-MTAB-7077 | ExpressionAtlas

AATF/Che-1 binds ribosome-associated RNAs and regulates ribosome biogenesis

Project description:AATF is a predominantly nuclear protein that has been shown to be an apoptosis-inhibiting factor essential for both embryonic development and tumor growth. Several studies have shown a role of AATF in the modulation of pivotal cellular signal transduction pathways such as p53-, mTOR- and HIF-signaling. However, the exact molecular functions underlying its essential nature to cell proliferation and survival have remained elusive. Interestingly, several lines of evidence point towards a pivotal role of this protein in ribosome biogenesis and the maturation of ribosomal RNA. The function of AATF in this process is not clear, especially since the identity of the RNA-binding protein that links the AATF-containing protein complex (ANN) to rRNA precursors is unknown. In this study, we identify AATF in a screen for RNA-binding proteins. Importantly, AATF does not only bind to polyA-tailed RNA but CLIP-experiments reveal its association with ribosomal RNA. The RNA-binding domain of AATF is essential to maintain its positive effect on cellular rRNA levels. Furthermore, AATF binds to both mRNAs encoding for ribosome biogenesis factors as well as proteins involved with this process indicating AATF to be a central hub for the coordination of ribosome maturation. Consequently, our data for the first time identify the molecular basis to the role of AATF in ribosome biosynthesis and corroborate the link between tumorigenesis and ribosome biology.

2019-08-13 | PXD011055 | Pride

Effect of AATF silencing on gene expression of BIU-87 [RNA-seq]

Project description:Differentially expressed genes were identified by comparing the gene expression profiling of BIU-87 of AATF silencing with that of control. Results provide important information to indicate Effect of AATF silencing on BIU-87.

2023-11-22 | GSE248071 | GEO

AATF/Che-1 localizes to paraspeckles and suppresses R-loops accumulation and interferon activation in Multiple Myeloma

Project description:We investigated the interactions of AATF/Che1 with paraspeckles complex in Multiple Myeloma(MM) cells by looking at its relationship with lncRNA NEAT1_1(NEAT1) and the essential paraspeckles proteins. By analyzing ChIP- and ChIRP-sequencing of MM cells, we assessed that the interaction between AATF/Che1 and NEAT1 occurs also onto DNA and detected the sites where they co-localize. To better characterize the interaction, we studied the effects of interfering AATF/Che1 or NEAT1 on co-localizing sites through ChIP-seq with NEAT1 interfered (GapmerNEAT1) and ChIRP-seq with AATF/Che1 interfered (siChe). We found that NEAT1 is essential in maintaining the paraspeckles complex onto those sites. Moreover, by exploring DRIP-seq data with siChe, we also detected that AATF/Che1 and NEAT1 localize on R-loops, RNA:DNA hybrid structure involved in DNA transcription and repair. A depletion of AATF/Che1 causes a further increase of those hybrid structures and the activation of the immune response in MM, in particular the interferon (IFN) activation. To further explore these findings, we performed RNA-seq with siChe and GapmerNEAT1 which confirm that AATF/Che-1 down-regulation induces a strong up-regulation of genes involved in IFN response.

2022-07-06 | GSE178868 | GEO

Nucleolar AATF regulates c-Jun-mediated apoptosis.

Project description:The AP-1 transcription factor c-Jun has been shown to be essential for stress-induced apoptosis in several models. However, the molecular mechanisms underlying the proapoptotic activity of c-Jun are poorly understood. We identify the apoptosis-antagonizing transcription factor (AATF) as a novel nucleolar stress sensor, which is required as a cofactor for c-Jun-mediated apoptosis. Overexpression or down-regulation of AATF expression levels led to a respective increase or decrease in the amount of activated and phosphorylated c-Jun with a proportional alteration in the induction levels of the proapoptotic c-Jun target genes FasL and TNF-?. Accordingly, AATF promoted commitment of ultraviolet (UV)-irradiated cells to c-Jun-dependent apoptosis. Whereas AATF overexpression potentiated UV-induced apoptosis in wild-type cells, c-Jun-deficient mouse embryonic fibroblasts were resistant to AATF-mediated apoptosis induction. Furthermore, AATF mutants defective in c-Jun binding were also defective in inducing AP-1 activity and c-Jun-mediated apoptosis. UV irradiation induced a translocation of AATF from the nucleolus to the nucleus, thereby enabling its physical association to c-Jun. Analysis of AATF deletion mutants revealed that the AATF domains required for compartmentalization, c-Jun binding, and enhancement of c-Jun transcriptional activity were all also required to induce c-Jun-dependent apoptosis. These results identify AATF as a nucleolar-confined c-Jun cofactor whose expression levels and spatial distribution determine the stress-induced activity of c-Jun and the levels of c-Jun-mediated apoptosis.

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A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

Project description:A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

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Antagonizing IL-1β to treat GBM

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ChIP-seq following AATF in BIU-87 cells

Project description:ChIP-seq following AATF in BIU-87 cells

| PRJNA1043085 | ENA